427 research outputs found
ON COMPUTING UPPER LIMITS TO SOURCE INTENSITIES
A common problem in astrophysics is determining how bright a source could be
and still not be detected. Despite the simplicity with which the problem can be
stated, the solution involves complex statistical issues that require careful
analysis. In contrast to the confidence bound, this concept has never been
formally analyzed, leading to a great variety of often ad hoc solutions. Here
we formulate and describe the problem in a self-consistent manner. Detection
significance is usually defined by the acceptable proportion of false positives
(the TypeI error), and we invoke the complementary concept of false negatives
(the TypeII error), based on the statistical power of a test, to compute an
upper limit to the detectable source intensity. To determine the minimum
intensity that a source must have for it to be detected, we first define a
detection threshold, and then compute the probabilities of detecting sources of
various intensities at the given threshold. The intensity that corresponds to
the specified TypeII error probability defines that minimum intensity, and is
identified as the upper limit. Thus, an upper limit is a characteristic of the
detection procedure rather than the strength of any particular source and
should not be confused with confidence intervals or other estimates of source
intensity. This is particularly important given the large number of catalogs
that are being generated from increasingly sensitive surveys. We discuss the
differences between these upper limits and confidence bounds. Both measures are
useful quantities that should be reported in order to extract the most science
from catalogs, though they answer different statistical questions: an upper
bound describes an inference range on the source intensity, while an upper
limit calibrates the detection process. We provide a recipe for computing upper
limits that applies to all detection algorithms.Comment: 30 pages, 12 figures, accepted in Ap
Alien Registration- Parent, Joseph B. (Van Buren, Aroostook County)
https://digitalmaine.com/alien_docs/32354/thumbnail.jp
An international comparative study of blood pressure in populations of European vs. African descent
Background: The consistent finding of higher prevalence of hypertension in US blacks compared
to whites has led to speculation that African-origin populations are particularly susceptible to this
condition. Large surveys now provide new information on this issue.
Methods: Using a standardized analysis strategy we examined prevalence estimates for 8 white
and 3 black populations (N = 85,000 participants).
Results: The range in hypertension prevalence was from 27 to 55% for whites and 14 to 44% for
blacks.
Conclusions: These data demonstrate that not only is there a wide variation in hypertension
prevalence among both racial groups, the rates among blacks are not unusually high when viewed
internationally. These data suggest that the impact of environmental factors among both
populations may have been under-appreciated
Serotonin tranporter methylation and response to cognitive behaviour therapy in children with anxiety disorders
Anxiety disorders that are the most commonly occurring psychiatric disorders in childhood, are associated with a range of social and educational impairments and often continue into adulthood. Cognitive behaviour therapy (CBT) is an effective treatment option for the majority of cases, although up to 35-45% of children do not achieve remission. Recent research suggests that some genetic variants may be associated with a more beneficial response to psychological therapy. Epigenetic mechanisms such as DNA methylation work at the interface between genetic and environmental influences. Furthermore, epigenetic alterations at the serotonin transporter (SERT) promoter region have been associated with environmental influences such as stressful life experiences. In this study, we measured DNA methylation upstream of SERT in 116 children with an anxiety disorder, before and after receiving CBT. Change during treatment in percentage DNA methylation was significantly different in treatment responders vs nonresponders. This effect was driven by one CpG site in particular, at which responders increased in methylation, whereas nonresponders showed a decrease in DNA methylation. This is the first study to demonstrate differences in SERT methylation change in association with response to a purely psychological therapy. These findings confirm that biological changes occur alongside changes in symptomatology following a psychological therapy such as CBT
Identification of plasma lipid biomarkers for prostate cancer by lipidomics and bioinformatics
Background:
Lipids have critical functions in cellular energy storage, structure and signaling. Many individual lipid molecules have been associated with the evolution of prostate cancer; however, none of them has been approved to be used as a biomarker. The aim of this study is to identify lipid molecules from hundreds plasma apparent lipid species as biomarkers for diagnosis of prostate cancer.
Methodology/Principal Findings:
Using lipidomics, lipid profiling of 390 individual apparent lipid species was performed on 141 plasma samples from 105 patients with prostate cancer and 36 male controls. High throughput data generated from lipidomics were analyzed using bioinformatic and statistical methods. From 390 apparent lipid species, 35 species were demonstrated to have potential in differentiation of prostate cancer. Within the 35 species, 12 were identified as individual plasma lipid biomarkers for diagnosis of prostate cancer with a sensitivity above 80%, specificity above 50% and accuracy above 80%. Using top 15 of 35 potential biomarkers together increased predictive power dramatically in diagnosis of prostate cancer with a sensitivity of 93.6%, specificity of 90.1% and accuracy of 97.3%. Principal component analysis (PCA) and hierarchical clustering analysis (HCA) demonstrated that patient and control populations were visually separated by identified lipid biomarkers. RandomForest and 10-fold cross validation analyses demonstrated that the identified lipid biomarkers were able to predict unknown populations accurately, and this was not influenced by patient's age and race. Three out of 13 lipid classes, phosphatidylethanolamine (PE), ether-linked phosphatidylethanolamine (ePE) and ether-linked phosphatidylcholine (ePC) could be considered as biomarkers in diagnosis of prostate cancer.
Conclusions/Significance:
Using lipidomics and bioinformatic and statistical methods, we have identified a few out of hundreds plasma apparent lipid molecular species as biomarkers for diagnosis of prostate cancer with a high sensitivity, specificity and accuracy
The Eyes Have It: Sex and Sexual Orientation Differences in Pupil Dilation Patterns
Recent research suggests profound sex and sexual orientation differences in sexual response. These results, however, are based on measures of genital arousal, which have potential limitations such as volunteer bias and differential measures for the sexes. The present study introduces a measure less affected by these limitations. We assessed the pupil dilation of 325 men and women of various sexual orientations to male and female erotic stimuli. Results supported hypotheses. In general, self-reported sexual orientation corresponded with pupil dilation to men and women. Among men, substantial dilation to both sexes was most common in bisexual-identified men. In contrast, among women, substantial dilation to both sexes was most common in heterosexual-identified women. Possible reasons for these differences are discussed. Because the measure of pupil dilation is less invasive than previous measures of sexual response, it allows for studying diverse age and cultural populations, usually not included in sexuality research
The Contribution of Cancer Incidence, Stage at Diagnosis and Survival to Racial Differences in Years of Life Expectancy
African Americans have higher cancer mortality rates than whites. Understanding the relative contribution of cancer incidence, stage at diagnosis and survival after diagnosis to the racial gap in life expectancy has important implications for directing future health disparity interventions toward cancer prevention, screening and treatment.
We estimated the degree to which higher cancer mortality among African Americans is due to higher incidence rates, later stage at diagnosis or worse survival after diagnosis.
Stochastic model of cancer incidence and survival after diagnosis.
Surveillance and Epidemiology End Result cancer registry and National Health Interview Survey data.
Life expectancy if African Americans had the same cancer incidence, stage and survival after diagnosis as white adults.
African-American men and women live 1.47 and 0.91 fewer years, respectively, than whites as the result of all cancers combined. Among men, racial differences in cancer incidence, stage at diagnosis and survival after diagnosis account for 1.12 (95% CI: 0.52 to 1.36), 0.17 (95% CI: −0.03 to 0.33) and 0.21 (95% CI: 0.05 to 0.34) years of the racial gap in life expectancy, respectively. Among women, incidence, stage and survival after diagnosis account for 0.41 (95% CI: −0.29 to 0.60), 0.26 (95% CI: −0.06 to 0.40) and 0.31 (95% CI: 0.05 to 0.40) years, respectively. Differences in stage had a smaller impact on the life expectancy gap compared with the impact of incidence. Differences in cancer survival after diagnosis had a significant impact for only two cancers—breast (0.14 years; 95% CI: 0.05 to 0.16) and prostate (0.05 years; 95% CI 0.01 to 0.09).
In addition to breast and colorectal cancer screening, national efforts to reduce disparities in life expectancy should also target cancer prevention, perhaps through smoking cessation, and differences in survival after diagnosis among persons with breast and prostate cancer
Microfluidic Perfusion for Regulating Diffusible Signaling in Stem Cells
Background
Autocrine & paracrine signaling are widespread both in vivo and in vitro, and are particularly important in embryonic stem cell (ESC) pluripotency and lineage commitment. Although autocrine signaling via fibroblast growth factor-4 (FGF4) is known to be required in mouse ESC (mESC) neuroectodermal specification, the question of whether FGF4 autocrine signaling is sufficient, or whether other soluble ligands are also involved in fate specification, is unknown. The spatially confined and closed-loop nature of diffusible signaling makes its experimental control challenging; current experimental approaches typically require prior knowledge of the factor/receptor in order to modulate the loop. A new approach explored in this work is to leverage transport phenomena at cellular resolution to downregulate overall diffusible signaling through the physical removal of cell-secreted ligands.
Methodology/Principal Findings
We develop a multiplex microfluidic platform to continuously remove cell-secreted (autocrine\paracrine) factors to downregulate diffusible signaling. By comparing cell growth and differentiation in side-by-side chambers with or without added cell-secreted factors, we isolate the effects of diffusible signaling from artifacts such as shear, nutrient depletion, and microsystem effects, and find that cell-secreted growth factor(s) are required during neuroectodermal specification. Then we induce FGF4 signaling in minimal chemically defined medium (N2B27) and inhibit FGF signaling in fully supplemented differentiation medium with cell-secreted factors to determine that the non-FGF cell-secreted factors are required to promote growth of differentiating mESCs.
Conclusions/Significance
Our results demonstrate for the first time that flow can downregulate autocrine\paracrine signaling and examine sufficiency of extracellular factors. We show that autocrine\paracrine signaling drives neuroectodermal commitment of mESCs through both FGF4-dependent and -independent pathways. Overall, by uncovering autocrine\paracrine processes previously hidden in conventional culture systems, our results establish microfluidic perfusion as a technique to study and manipulate diffusible signaling in cell systems.National Institutes of Health (U.S.) (NIH grant No. EB007278)Swiss National Science FoundationSwiss National Science Foundatio
- …